Kawakami J, Katakami C, Yamamoto M
Department of Ophthalmology, Kobe National Hospital, Hyogo ken, Japan.
Nippon Ganka Gakkai Zasshi. 1996 Sep;100(9):653-9.
To elucidate the mechanisms by which corneal sensory denervation causes corneal epithelial disorders, we investigated corneal epithelial changes in rats injected with capsaicin, which is known to desensitize the primary sensory neurons. Neonatal rats were injected with capsaicin (100 mg/kg) or only the vehicle as a control on the 2nd day after birth. Corneas were excised after 7-28 days and subjected to gold chloride staining. 3H-thymidine autoradiography, or immunohistochemistry using anti-substance P (SP) antibody. The results indicated poor attachment of corneal epithelium, decreased corneal nerve ending density, decreased 3H-thymidine uptake by epithelial cells, and decreased expression of SP in the epithelial layer in rats injected with capsaicin compared with the control rats. This suggests that decreased proliferation of corneal epithelial cells associated with decreased SP as well as poor attachment of the epithelium is one of the causes of neuroparalytic keratopathy.
为了阐明角膜感觉神经去支配导致角膜上皮疾病的机制,我们研究了注射辣椒素的大鼠的角膜上皮变化,已知辣椒素会使初级感觉神经元脱敏。新生大鼠在出生后第2天注射辣椒素(100mg/kg)或仅注射赋形剂作为对照。7-28天后切除角膜,进行氯化金染色、3H-胸腺嘧啶核苷放射自显影或使用抗P物质(SP)抗体的免疫组织化学。结果表明,与对照大鼠相比,注射辣椒素的大鼠角膜上皮附着不良、角膜神经末梢密度降低、上皮细胞对3H-胸腺嘧啶核苷的摄取减少以及上皮层中SP的表达降低。这表明与SP减少相关的角膜上皮细胞增殖减少以及上皮附着不良是神经麻痹性角膜病变的原因之一。